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目的 观察暂短性脑缺血再灌注后沙土鼠海马区谷氨酸的表达变化以及氟桂利嗪干预的影响。方法 按照Kirino的方法 ,制作缺血再灌注模型。于缺血再灌注后 1、2、7天采取免疫组化方法检测谷氨酸表达 ,并于 7天在电镜和光镜下观察组织学变化。结果 缺血再灌注组 1天及 2天海马CA1区谷氨酸表达增高 (P <0 .0 1) ,7天恢复正常。光镜及电镜可见给药组存活的神经元数目明显多于缺血再灌注组 (P <0 .0 1)。结论 谷氨酸表达增高可能是鼠脑海马区迟发性神经元死亡的原因之一 ,氟桂利嗪可抑制谷氨酸的表达 ,对缺血的神经元起保护作用。
Objective To observe the changes of glutamate expression in hippocampus of transient gerbil after transient focal cerebral ischemia and the effect of flunarizine intervention. Methods According to Kirino’s method, a model of ischemia-reperfusion was made. The expression of glutamate was detected by immunohistochemical method on the 1st, 2nd, 7th day after ischemia reperfusion. The histological changes were observed under electron microscope and light microscope on the 7th day. Results The expression of glutamate in hippocampus CA1 area increased (P <0.01) on day 1 and day 2 in ischemia-reperfusion group and returned to normal in 7 days. Light and electron microscopy showed that the number of neurons in the drug-treated group was significantly more than that in the ischemia-reperfusion group (P <0.01). Conclusion The increased expression of glutamate may be one of the reasons for the delayed neuronal death in the hippocampus of rats. Flunarizine can inhibit the expression of glutamate and protect the ischemic neurons.